Delayed growth of EL4 lymphoma in SR‐A‐deficient mice is due to upregulation of nitric oxide and interferon‐γ production by tumor‐associated macrophages
書誌事項
- 公開日
- 2009-10-11
- 資源種別
- journal article
- 権利情報
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- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
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- 10.1111/j.1349-7006.2009.01296.x
- 公開者
- Wiley
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説明
<jats:p>Class A scavenger receptors (SR‐A, CD204) are highly expressed in tumor‐associated macrophages (TAM). To investigate the function of SR‐A in TAM, wild‐type and SR‐A‐deficient (SR‐A<jats:sup>−/−</jats:sup>) mice were injected with EL4 cells. Although these groups of mice did not differ in the numbers of infiltrating macrophages and lymphocytes and in neovascularization, SR‐A<jats:sup>−/−</jats:sup> mice had delayed growth of EL4 tumors. Expression of inducible nitric oxide (NO) synthase and interferon (IFN)‐γ mRNA increased significantly in tumor tissues from SR‐A<jats:sup>−/−</jats:sup> mice. Engulfment of necrotic EL4 cells induced upregulation of NO and IFN‐γ production by cultured macrophages, and production of NO and IFN‐γ increased in SR‐A<jats:sup>−/−</jats:sup> macrophages <jats:italic>in vitro</jats:italic>. IFN‐β production by cultured macrophages was also elevated in SR‐A<jats:sup>−/−</jats:sup> macrophages <jats:italic>in vitro</jats:italic>. These results suggested that the antitumor activity of macrophages increased in SR‐A<jats:sup>−/−</jats:sup> mice because of upregulation of NO and IFN‐γ production. These data indicate an important role of SR‐A in regulating TAM function by inhibiting toll‐like receptor (TLR)4–IFN‐β signaling. (<jats:italic>Cancer Sci</jats:italic> 2009); 00: 000–000)</jats:p>
収録刊行物
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- Cancer Science
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Cancer Science 100 (11), 2160-2166, 2009-10-11
Wiley
